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Abstract <p>Increased intestinal pain sensitivity (intestinal hyperalgesia)can be a consequence of intestinal inflammation or prior stress.Both conditions are thought to be associated with a dysfunctionof the basolateral amygdala (BLA), as they are accompanied by neurochemicaland molecular changes in this structure. However, the concomitantalterations in the neuronal mechanisms of BLA-mediated control ofvisceral nociception and their potential specificity for post-inflammatoryand stress-induced hyperalgesia remain unclear. The aim of thisstudy was to comparatively assess changes in the functional propertiesof visceral pain-responsive BLA neurons and their modulation bythe infralimbic region of the medial prefrontal cortex (IL), whichoccur after intestinal inflammation or stress. The study was carried outon male Wistar rats divided into three groups: (1) controls, (2)those recovered from experimental colitis, and (3) those exposedto prolonged emotional-painful stress. In awake rats from all groups, intestinalhyperalgesia was assessed by recording the visceromotor responsesto noxious colorectal distension (CRD), while in anesthetized animals,the background activity of BLA neurons and their responses to CRDbefore and after electrical stimulation of the IL was evaluatedby microelectrode recording. It was found that post-colitis andstressed rats exhibited intestinal hyperalgesia, which was morepronounced in the latter. The post-colitis conditions were associatedwith a decrease while the post-stress conditions—with an increasein the background firing rate of BLA neurons. For the first time, itwas shown that in both cases, the reactivity of BLA neurons respondingto CRD with an excitation or inhibition to the activating effectsof the IL was enhanced. However, the post-colitis period was characterizedby an increase in the activating effect of the IL on CRD-inhibitedBLA neurons, while the post-stress period was marked by an increasein the stimulating effect of the IL on both excited and inhibitedBLA nociceptive neurons. The neuronal alterations, revealed in theBLA, may lead to disruptions in the amygdaloid control of the sensoryand emotional components of visceral pain, inherent in post-inflammatoryor post-stress intestinal hyperalgesia, being thus a potential targetin the treatment of the latter in clinical practice.</p>

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The Features of Neural Mechanisms Underlying Visceral Pain Processing in the Basolateral Amygdala of Rats with Post-Inflammatory or Stress-Induced Hyperalgesia

  • 期刊论文

  • 发表日期：

    2025年7月1日

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  • O. A. Lyubashina,
  • D. A. Mehilyainen,
  • I. B. Sivachenko

摘要

Abstract

Increased intestinal pain sensitivity (intestinal hyperalgesia)can be a consequence of intestinal inflammation or prior stress.Both conditions are thought to be associated with a dysfunctionof the basolateral amygdala (BLA), as they are accompanied by neurochemicaland molecular changes in this structure. However, the concomitantalterations in the neuronal mechanisms of BLA-mediated control ofvisceral nociception and their potential specificity for post-inflammatoryand stress-induced hyperalgesia remain unclear. The aim of thisstudy was to comparatively assess changes in the functional propertiesof visceral pain-responsive BLA neurons and their modulation bythe infralimbic region of the medial prefrontal cortex (IL), whichoccur after intestinal inflammation or stress. The study was carried outon male Wistar rats divided into three groups: (1) controls, (2)those recovered from experimental colitis, and (3) those exposedto prolonged emotional-painful stress. In awake rats from all groups, intestinalhyperalgesia was assessed by recording the visceromotor responsesto noxious colorectal distension (CRD), while in anesthetized animals,the background activity of BLA neurons and their responses to CRDbefore and after electrical stimulation of the IL was evaluatedby microelectrode recording. It was found that post-colitis andstressed rats exhibited intestinal hyperalgesia, which was morepronounced in the latter. The post-colitis conditions were associatedwith a decrease while the post-stress conditions—with an increasein the background firing rate of BLA neurons. For the first time, itwas shown that in both cases, the reactivity of BLA neurons respondingto CRD with an excitation or inhibition to the activating effectsof the IL was enhanced. However, the post-colitis period was characterizedby an increase in the activating effect of the IL on CRD-inhibitedBLA neurons, while the post-stress period was marked by an increasein the stimulating effect of the IL on both excited and inhibitedBLA nociceptive neurons. The neuronal alterations, revealed in theBLA, may lead to disruptions in the amygdaloid control of the sensoryand emotional components of visceral pain, inherent in post-inflammatoryor post-stress intestinal hyperalgesia, being thus a potential targetin the treatment of the latter in clinical practice.